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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A gross, light, and electron microscopic study of the eyes from 35 consecutive autopsy cases of the acquired immune deficiency syndrome revealed cotton-wool spots (71% of cases), retinal hemorrhage in areas without cytomegalovirus infection (40%), cytomegalovirus retinitis (34%) with associated retinal detachment, Roth's spots (23%), retinal microaneurysms (20%), papilledema (14%), conjunctival Kaposi's sarcoma (9%), cryptococcal chorioretinitis (6%), Mycobacterium avium-intracellulare in retina and in choroidal granulomas (6%), ischemic maculopathy (6%), bilateral keratitis (3%), and herpes simplex retinitis (3%). Ocular infection with candida or toxoplasmosis were not found in this autopsy series. Immunocytologic studies demonstrated deposition of immunoglobulins in arteriolar walls, consistent with immune complex mediated disease. Ultrastructural studies showed a vasculopathy in the areas near cotton-wool spots. A mechanism is proposed linking the deposition of immune complexes with subsequent small vessel lesions, ischemia, cotton-wool spots and later spread of cytomegalovirus to retina via damaged vascular endothelium.
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PMID:Acquired immune deficiency syndrome. Pathogenic mechanisms of ocular disease. 298 69

The normal bacterial flora of the skin represents an important host defense mechanism against invasion by potentially pathogenic organisms. This flora is primarily composed of aerobic diphtheroids (Corynebacterium species), anaerobic diphtheroids (Propriono-bacterium acnes), and coagulase-negative staphylococci. Gram-negative bacilli may be present in limited numbers in intertriginous areas. Localized cutaneous infections occur in ostensibly normal hosts, often after trivial trauma, examples being streptococcal or staphylococcal impetigo, staphylococcal furunculosis, or more unusual infections due to agents such as Mycobacterium marinum. When the skin is injured more extensively by trauma, burns, ischemia with ulceration, or iatrogenic manipulations, or when host immunologic defenses are suppressed, more severe infections are likely to supervene, and the threat of systemic dissemination of infecting microorganisms increases. Cutaneous infection in immunosuppressed hosts may involve the same pyogenic bacteria that affect normal subjects or it may involve a variety of opportunistic invaders, including herpes viruses, gram-negative bacilli, mycobacteria, and deep or superficial mycoses. The skin may also be affected by infections whose primary site lies elsewhere in the body. Cutaneous manifestations may be secondary to hematogenous seeding of the causative agent or to the effects of toxins or immune complexes. Certain microbial agents may initiate a wide variety of cutaneous lesions, depending on route of infection and the status of the host. Thus, cutaneous lesions attributable to Pseudomonas aeruginosa range from "green nail syndrome" and self-limited folliculitis to ecthyma gangrenosum. Similarly, group A streptococci may produce pyoderma, cellulitis, lymphangitis, erysipelas, or scarlet fever. We recently described a syndrome of recurrent cellulitis in the saphenous vein donor extremities of patients who have undergone coronary artery bypass grafts. Most patients have associated tinea pedis. The pathophysiologic aspects of this syndrome are probably multifactorial, involving compromise of lymphatic or venous drainage, bacterial infection, elaboration of bacterial toxins, and hypersensitivity to bacterial or fungal products, or both. Coagulase-negative staphylococci are exhibiting a more prominent pathogenic potential than heretofore. When they infect immunosuppressed hosts or patients with indwelling intravascular catheters or cardiac prostheses, coagulase-negative staphylococci may cause life-threatening disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cutaneous infections: microbiologic and epidemiologic considerations. 637 67

Reperfusion injury, which occurs upon the reintroduction of blood flow to an ischemic organ, is responsible for considerable damage in heart attacks and strokes. However, no treatment for reperfusion injury is currently available. A major cause of reperfusion injury is the iron-mediated generation of hydroxyl radical (.OH). In this study we have explored the capacity of novel iron chelators called "exochelins" to prevent reperfusion injury. Exochelins, siderophores of Mycobacterium tuberculosis, are unique iron chelators because they are lipid soluble, and hence able to enter cells rapidly. In the iron-free state, exochelins prevented .OH formation. Desferri-exochelins prevented oxidative injury to cultured cardiac myocytes, and did so more rapidly and effectively than the nonlipid soluble iron chelator deferoxamine. The capacity of various desferri-exochelins to protect myocytes from oxidative injury varied directly with their solubility in lipid. Infused into isolated rabbit hearts during reperfusion after a period of ischemia, desferri-exochelins dramatically improved systolic and diastolic left ventricular function, preserved coronary flow, reduced release of the cardiac enzyme lactic dehydrogenase, and reduced myocardial concentrations of .OH metabolites. Thus, highly diffusible desferri-exochelins block injury caused by .OH production and have potential for the treatment of reperfusion injury.
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PMID:Lipophilic siderophores of Mycobacterium tuberculosis prevent cardiac reperfusion injury. 956 Feb 64

Infection of peripheral nerve by Mycobacterium leprae, the histopathological hallmark of leprosy, is a major factor in this disease, but the route and mechanisms by which bacilli localize to peripheral nerve are unknown. Experimentally infected armadillos have recently been recognized as a model of lepromatous neuritis; the major site of early accumulation of M. leprae is epineurial. To determine the epineurial cells involved, 1-cm segments of 44 nerves from armadillos were screened for acid-fast bacilli and thin sections were examined ultrastructurally. Of 596 blocks containing nerve, 36% contained acid-fast bacilli. Overall, M. leprae were found in endothelial cells in 40% of epineurial blood vessels and 75% of lymphatics, and in 25% of vessels intraneurally. Comparison of epineurial and endoneurial findings suggested that colonization of epineurial vessels preceded endoneurial infection. Such colonization of epineurial nutrient vessels may greatly increase the risk of endoneurial M. leprae bacteremia, and also enhance the risk of ischemia following even mild increases in inflammation or mechanical stress. These findings also raise the possibility that early, specific mechanisms in the localization of M. leprae to peripheral nerve may involve adhesion events between M. leprae (or M. leprae-parasitized macrophages) and the endothelial cells of the vasa nervorum.
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PMID:Localization of Mycobacterium leprae to endothelial cells of epineurial and perineurial blood vessels and lymphatics. 1032 13

Medical treatment of Buruli ulcer is mostly disappointing even if Mycobacterium ulcerans is susceptible to many antibacterial drugs. The inefficiency in vivo of the drugs may be due to the tissue vascularisation disorders caused by the toxin that Mycobacterium ulcerans produces. This toxin causes an endarteritis followed by a thrombosis of the dermal vessels responsible for an ischemia which prevents the antibacterial drugs from reaching the infected area. Removal or prevention of that thrombosis should allow the drugs to be more effective. To verify this assumption, we used a combined therapy with two gold standard medicines in an oedematous form of Buruli ulcer on the face which could not be surgically treated: heparin for its activity on thrombosis and rifampin for its bactericidal activity on Mycobacterium ulcerans. Rifampin was administered at 300 mg dose per day. Based on the management of envenomisation cases due to viper bites, we used standard heparin at 500 Ul dose per kg repeatedly administered by an electrical syringe releasing 1 cc per hour in the tubulure of isotonic glucose infusion. The results were encouraging. The dreadful oedema of the face started to reduce on the 15th day and disappeared on the 30th day. A small area at the temple dried. But we were obliged to stop the use of standard heparin due to an occurrence of Klebsiella oxytoca septicaemia from permanent vein route. Rifampin was still administered at the same dose. The face oedema reappeared quickly, followed by a full closure of the eyelids and an ulceration at the right temple level. The standard heparin was therefore substituted by low weight molecular heparin, enoxaparin, administered at 40 mg twice per day by subcutaneous route. 45 days later the oedema reduced and ulceration did not develop. After 90 days of treatment, usual signs of mycobacterial infection progression disappeared. We stopped therefore the use of enoxaparin but continued with rifampin until healing of the ulceration which occurred after 12 months of treatment. We observed no recurrence over a period of 16 months after complete healing. We can conclude that heparin combined with antimycobacterial drugs--which are active in vitro on Mycobacterium ulcerans--could provide an effective medical treatment for Buruli ulcer.
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PMID:[Contribution of heparin therapy in the medical treatment of Buruli ulcer apropos of 1 case]. 1134 80

Ileitis, or inflammation of the ileum, is often caused by Crohn's disease. However, ileitis may be caused by a wide variety of other diseases. These include infectious diseases, spondyloarthropathies, vasculitides, ischemia, neoplasms, medication-induced, eosinophilic enteritis, and others. The clinical presentation of ileitis may vary from an acute and self-limited form of right lower quadrant pain and/or diarrhea, as in the majority of cases of bacterial ileitis, but some conditions (ie, vasculitis or Mycobacterium tuberculosis) follow a chronic and debilitating course complicated by obstructive symptoms, hemorrhage, and/or extraintestinal manifestations. Ileitis associated with spondylarthropathy or nonsteroidal anti-inflammatory drugs is typically subclinical and often escapes detection unless further testing is warranted by symptoms. In a minority of patients with long-standing Crohn's ileitis, the recrudescence of symptoms may represent a neoplasm involving the ileum. Distinguishing between the various forms of ileitis remains a test of clinical acumen. The diagnosis of the specific etiology is suggested by a detailed history and physical examination, laboratory testing, and ileocolonoscopy and/or radiologic data.
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PMID:Ileitis: when it is not Crohn's disease. 2053 6

Eales' disease, first described by the British ophthalmologist Henry Eales in 1880, is characterized by three overlapping stages of venous inflammation (vasculitis), occlusion, and retinal neovascularization. Diagnosis is mostly clinical and requires exclusion of other systemic or ocular conditions that could present with similar retinal features. In recent years, immunological, molecular biological, and biochemical studies have indicated the role of human leukocyte antigen, retinal autoimmunity, Mycobacterium tuberculosis genome, and free radical-mediated damage in the etiopathogenesis of this disease. However, its etiology appears to be multifactorial. The management depends on the stage of the disease and consists of medical treatment with oral corticosteroids in the active inflammatory stage and laser photocoagulation in the advanced retinal ischemia and neovascularization stages.
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PMID:Eales' disease - current concepts in diagnosis and management. 2351 27

A systematic ultrastructure of peripheral nerves across the spectrum of leprosy was studied with an aim to better understanding the pathogenesis of nerve involvement in leprosy using light and electron microscope. The pathogenesis of nerve destruction varies in leprosy considerably along the spectrum. The study has begun to shed new light on some aspects of the infection of Mycobacterium leprae (M. lepare) and phenomenon has opened new avenue of research and possible mechanism of pathogenesis in TT/BT/BL/LL leprosy. In tuberculoid type (TT) and borderline tuberculoid (BT) leprosy, the degenerative changes of Schwann cells (SCs) and presence of perineural and perivascular cuffing by mononuclear cells. The endoneurial blood vessel (EBV) showed thickening of basement membrane with hypertrophy of EC leading to narrowing or complete occlusion of lumen and causing ischemia. However, borderline lepromatous (BL) and lepromatous leprosy (LL) foamy macrophages and vacuolated SC contain numerous small dense materials, irregular in shape and size was prominent and, considered to be degenerated and fragmented M. Leprae. The dense materials were also found in the cytoplasm of vascular EC. It was revealed that besides SC, the EC of EBV frequently harbor M. leprae in LL. The lumen of the EBV was wide open with enlarged nucleus. In the present study, the ultrastructural characteristics suggest that hypersensitivity mechanisms are possibly responsible for nerve damage in TT/BT leprosy. However, the study indicates that the mechanisms of nerve damage in BL/LL are basically different wherein hypersensitivity appears to play a very limited role.
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PMID:High resolution structural changes of Schwann cell and endothelial cells in peripheral nerves across leprosy spectrum. 2446 Jul 57

A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2 ng/ml and as early as 8 hrs after exposure. TM activates protein C by altering thrombin's substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells' ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone's effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tissue ischemia could contribute to the development of the tissue necrosis seen in BU lesions.
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PMID:Mycolactone-Dependent Depletion of Endothelial Cell Thrombomodulin Is Strongly Associated with Fibrin Deposition in Buruli Ulcer Lesions. 2618 60

The syndrome of recurrent vitreous hemorrhages in young men was described for the first time by Henry Eales in 1880. The association with a clinical manifestation of ocular inflammation was reported 5years later. Eales disease affects young adults who present with ischemic retinal vasculitis, with the peripheral retina most commonly affected. Most cases have been reported in South Asia. Although the etiology of this abnormality is unknown, it may be related to an immune sensitivity to Mycobacterium tuberculosis antigens. Its pathogenesis is related to extensive ischemia that affects the retina, secondary to an obliterative retinal vasculopathy with release of angiogenic factors of the VEGF type. Involvement of the retina is the hallmark of the disease, which manifests as follows: periphlebitis, retinal capillary ischemia most often affecting the periphery with secondary proliferative retinopathy and retinal and/or papillary neovascularization, recurrent vitreous hemorrhages and tractional retinal detachment. These complications are potentially blinding. The natural history of Eales disease varies, with temporary or permanent remission in some cases and continuous progression in others. Progression is often bilateral, which necessitates regular follow-up. The treatment of Eales disease depends on the stage of the disease and is not well defined. Observation only, pars plana vitrectomy surgery and/or intravitreal injections of anti-VEGF are recommended in cases of vitreous hemorrhage, associated with corticosteroids when retinal vasculitis is present. Laser pan-retinal photocoagulation is necessary when neovascularization is present.
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PMID:[Eales' disease]. 2718 61


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